Gold nephropathy. Ultrastructural, fluorescent, and energy-dispersive x-ray microanalysis study.
The nephrotic syndrome developed in a patient receiving therapy with gold for rheumatoid arthritis. The results of a histopathological examination of the renal biopsy specimen were unremarkable. Immunofluorescent studies showed deposits of immunoglobulins and C3 in a granular pattern in the glomerular basement membranes. Ultrastructurally, the discrete osmiophilic immune complexes were epimembranous. By x-ray microanalysis, gold that was complexed with sulfur was present in proximal tubular cytoplasmic vacuoles and nuclei. Gold and sulfur could not be demonstrated in glomerular epimembranous deposits. The results of these studies suggest that immune complex deposition does not involve gold and sulfur acting as haptens. Gold-salt therapy may result in damage to proximal tubules that leak renal tubular antigens, which in turn complex with autoantibody and produce an autoimmune membranous nephropathy. The evidence for this mechanism is not convincing. Although the data indicate an immune-complex cause for gold-salt nephropathy, the incident antigen (or antigens) and mechanism of action remain unidentified.
D000328:Adult; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D004577:Electron Probe Microanalysis; D005260:Female; D005455:Fluorescent Antibody Technique; D006052:Gold Sodium Thiomalate / Q000009:adverse effects*; D006801:Humans; D007684:Kidney Tubules / Q000032:analysis; D009404:Nephrotic Syndrome / Q000139:chemically induced* / Q000000981:diagnostic imaging; D011859:Radiography
D006052:Gold Sodium Thiomalate